The project will analyze the anatomical substrates of oculomotor integration related to the neostriatum (caudate nucleus specifically). Caudate nucleus is strongly implicated in eye movement control by virtue of (i) afferent and efferent connections with many CNS regions of identified oculomotor function, (ii) specific eye movement disorders associated with basal ganglia disease, and (iii) experimental observations directly linking the strio-nigral and nigro-tectal pathways with higher order contingencies of eye movement control. The first aim of the project is to analyze the organization of striatum with respect to the distributions of corticostriate projections originating from identified visuomotor cortical areas. This will involve (i) determining whether caudate contains specific foci of convergence of visuomotor corticostriate projections, (ii) mapping the distribution of these foci, and (iii) determining the degree of overlap within caudate of multiple converging visuomotor cortical inputs. This aim will be addressed by mapping focal evoked potentials elicited by direct electrical stimulation of cortical visuomotor areas to identify the distribution of corticostriatal projections and their co-distributions considered 2 and 3 at a time. The second aim is to study the connections of the identified striatal foci in order to analyze their overall patterns of connectivity with other identified oculomotor regions. Caudate foci identified as receiving converging visuomotor cortical inputs will be injected with 3H-amino acid and with WGA conjugated HRP to study the pattern of their efferent and afferent connections. Analysis of these anatomical connections will permit detailed descriptions of important, and largely unexplored, anatomical substrates of the higher order eye movement control subsystems. The long term objective of this approach is to employ the basic anatomical "wiring diagram" to develop a predictive model of cortical and striatal contribution to oculomotor control. It is expected that this approach will eventually (i) shed new light on the role of higher centers in oculomotor control, (ii) predict new underlying principles of control which will be amenable to direct experimental tests, and (iii) explain some underlying mechanisms of clinical oculomotor syndromes related to cortical damage, basal ganglia disease, and congenital apraxias. The long term consequences of such an approach should be an improvement in methods of diagnosis and treatment of many debilitating oculomotor disorders.